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已发表论文
miR-574-3p在急性胰腺炎中的诊断和预后价值：来自生物信息学和体外研究的见解
Authors Wu X, Gong D, Cheng L, Zhou J
Received 9 June 2025
Accepted for publication 18 November 2025
Published 17 January 2026 Volume 2026:19 542184
DOI https://doi.org/10.2147/JIR.S542184
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Ning Quan
Xueyan Wu, Danfeng Gong, Long Cheng, Jing Zhou
Department of Gastroenterology, Changde Hospital, Xiangya School of Medicine, Central South University (The First People’s Hospital of Changde City), Changde, Hunan, People’s Republic of China
Correspondence: Jing Zhou, Department of Gastroenterology, Changde Hospital, Xiangya School of Medicine, Central South University (The first People’s Hospital of Changde City), 818 Renmin Road, Changde, Hunan, 415000, People’s Republic of China, Email Zhoujingchde@163.com
Background: MicroRNA (miRNA) exists great potential as a biomarker for various diseases.
Purpose: This study aimed to explore the role and mechanism of miR-574-3p in acute pancreatitis (AP) to improve clinical management.
Patients and Methods: Clinical data from 241 AP patients (87 mild (MAP), 154 moderate-severe (M/SAP)) and 77 healthy controls were analyzed. Dysregulated miRNAs were screened via GEO, with expression levels quantified by qRT-PCR. The miR-574-3p value in AP was assessed via ROC curves, correlation analysis, and multivariate logistic regression. Caerulein-induced HPDE6-C7 cell models were employed to evaluate the effects of miR-574-3p on proliferation, oxidative stress, and inflammation. Luciferase assays confirmed miR-574-3p/EGFR interaction.
Results: MiR-574-3p was downregulated in AP and lower in M/SAP than in MAP patients, demonstrating its diagnostic utility. MiR-574-3p was negatively associated with AP severity as evidenced by its correlation with the scoring systems, including Ranson, APACHE II, and SOFA, and served as a risk factor for poor prognosis of M/SAP. In vitro, miR-574-3p overexpression promoted cell proliferation, reduced oxidative stress (decreased MDA, increased SOD), and suppressed inflammation (IL-6, IL-1β, TNF-α) in caerulein-stimulated HPDE6-C7 injury model. EGFR was identified as a downstream gene of miR-574-3p, and its upregulation reversed the protective effects of miR-574-3p.
Conclusion: MiR-574-3p, associating with AP severity, served as a diagnostic biomarker for AP and M/SAP. MiR-574-3p was identified as a risk factor for the poor prognosis of M/SAP and involved in pancreatic cell injury through regulating EGFR. This work highlighted the clinical potential of miR-574-3p for AP diagnosis, prognosis and therapeutic strategies.
Keywords: acute pancreatitis, miR-574-3p, biomarker, EGFR, mechanism
Department of Gastroenterology, Changde Hospital, Xiangya School of Medicine, Central South University (The First People’s Hospital of Changde City), Changde, Hunan, People’s Republic of China
Correspondence: Jing Zhou, Department of Gastroenterology, Changde Hospital, Xiangya School of Medicine, Central South University (The first People’s Hospital of Changde City), 818 Renmin Road, Changde, Hunan, 415000, People’s Republic of China, Email Zhoujingchde@163.com
Background: MicroRNA (miRNA) exists great potential as a biomarker for various diseases.
Purpose: This study aimed to explore the role and mechanism of miR-574-3p in acute pancreatitis (AP) to improve clinical management.
Patients and Methods: Clinical data from 241 AP patients (87 mild (MAP), 154 moderate-severe (M/SAP)) and 77 healthy controls were analyzed. Dysregulated miRNAs were screened via GEO, with expression levels quantified by qRT-PCR. The miR-574-3p value in AP was assessed via ROC curves, correlation analysis, and multivariate logistic regression. Caerulein-induced HPDE6-C7 cell models were employed to evaluate the effects of miR-574-3p on proliferation, oxidative stress, and inflammation. Luciferase assays confirmed miR-574-3p/EGFR interaction.
Results: MiR-574-3p was downregulated in AP and lower in M/SAP than in MAP patients, demonstrating its diagnostic utility. MiR-574-3p was negatively associated with AP severity as evidenced by its correlation with the scoring systems, including Ranson, APACHE II, and SOFA, and served as a risk factor for poor prognosis of M/SAP. In vitro, miR-574-3p overexpression promoted cell proliferation, reduced oxidative stress (decreased MDA, increased SOD), and suppressed inflammation (IL-6, IL-1β, TNF-α) in caerulein-stimulated HPDE6-C7 injury model. EGFR was identified as a downstream gene of miR-574-3p, and its upregulation reversed the protective effects of miR-574-3p.
Conclusion: MiR-574-3p, associating with AP severity, served as a diagnostic biomarker for AP and M/SAP. MiR-574-3p was identified as a risk factor for the poor prognosis of M/SAP and involved in pancreatic cell injury through regulating EGFR. This work highlighted the clinical potential of miR-574-3p for AP diagnosis, prognosis and therapeutic strategies.
Keywords: acute pancreatitis, miR-574-3p, biomarker, EGFR, mechanism